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Neuroinflammation in Parkinson’s Disease Animal Models: A Cell Stress Response or a Step in Neurodegeneration?

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Book cover Behavioral Neurobiology of Huntington's Disease and Parkinson's Disease

Part of the book series: Current Topics in Behavioral Neurosciences ((CTBN,volume 22))

Abstract

The motor symptoms of Parkinson’s disease are due to the progressive degeneration of dopaminergic neurons in the substantia nigra. Multiple neuroinflammatory processes are exacerbated in Parkinson’s disease, including glial-mediated reactions, increased expression of proinflammatory substances, and lymphocytic infiltration, particularly in the substantia nigra. Neuroinflammation is also implicated in the neurodegeneration and consequent behavioral symptoms of many Parkinson’s disease animal models, although it is not clear whether these features emulate pathogenic steps in the genuine disorder or if some inflammatory features provide protective stress responses. Here, we compare and summarize findings on neuroinflammatory responses and effects on behavior in a wide range of toxin-based, inflammatory and genetic Parkinson’s disease animal models.

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Cebrián, C., Loike, J.D., Sulzer, D. (2014). Neuroinflammation in Parkinson’s Disease Animal Models: A Cell Stress Response or a Step in Neurodegeneration?. In: Nguyen, H., Cenci, M. (eds) Behavioral Neurobiology of Huntington's Disease and Parkinson's Disease. Current Topics in Behavioral Neurosciences, vol 22. Springer, Berlin, Heidelberg. https://doi.org/10.1007/7854_2014_356

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